The rest is silence.

Over the past several years, RNAi and its related phenomena have emerged not only as a powerful experimental tool but also as a new mode of gene regulation. Through a combination of genetic and biochemical approaches we have learned much about the mechanisms underlying dsRNA responses. However, many of the most intriguing aspects of dsRNA-induced gene silencing have yet to be illuminated. What has become abundantly clear is that the complex and highly conserved biology underlying RNA interference is critical both for genome maintenance and for the development of complex organisms. However, it seems probable that we have only begun to reveal the diversity of biological roles played by RNAi-related processes.     

Remembering silence.

Polycomb response elements (PREs) are regulatory switch elements that can direct the genes that they control to be either active or silenced. Once decided, this on or off state is maintained through subsequent cell divisions. We do not know how the switching works, or how it is copied to newly replicated chromosomes. Experiments that switch a silenced PRE to an active state have provided insights into both questions. A PRE switched experimentally can remember its previously silenced state and return to it after several cell divisions. In the most recent study of this phenomen on, the data show that several distinct variables affect the ability of PREs to "remember" and restore their previous state. The authors' interpretation of these results is discussed here.     

Spreading silence with Sid

RNA interference (RNAi) has been shown to spread from cell to cell in plants and in Caenorhabditis elegans, but it does not spread in other organisms, such as Drosophila. A recent report demonstrates that a membrane channel, encoded by the gene sid-1, is responsible for the spreading of RNAi between cells.     

Complexity beneath the silence

Polycomb group (PcG)-mediated silencing by proteins that are conserved across plants and animals is a key feature of eukaryotic gene regulation. Investigation of PcG-mediated gene silencing has revealed a surprising degree of complexity in the molecular mechanisms that recruit the protein complexes, repress expression, and maintain the epigenetic silent state of target genes. This review summarizes our current understanding of the mechanism of PcG-mediated gene silencing in animals and higher plants.     

The sound of silence: ionic mechanisms encoding sound termination

Offset responses upon termination of a stimulus are crucial for perceptual grouping and gap detection. These gaps are key features of vocal communication, but an ionic mechanism capable of generating fast offsets from auditory stimuli has proven elusive. Offset firing arises in the brainstem superior paraolivary nucleus (SPN), which receives powerful inhibition during sound and converts this into precise action potential (AP) firing upon sound termination. Whole-cell patch recording in?vitro showed that offset firing was triggered by IPSPs rather than EPSPs. We show that AP firing can emerge from inhibition through integration of large IPSPs, driven by an extremely negative chloride reversal potential (E(Cl)), combined with a large hyperpolarization-activated nonspecific cationic current (I(H)), with a secondary contribution from a T-type calcium conductance (I(TCa)). On activation by the IPSP, I(H) potently accelerates the membrane time constant, so when the sound ceases, a rapid repolarization triggers multiple offset APs that match onset timing accuracy.